scholarly journals Role of Gut Microbiota in Hepatocarcinogenesis

2019 ◽  
Vol 7 (5) ◽  
pp. 121 ◽  
Author(s):  
Haripriya Gupta ◽  
Gi Soo Youn ◽  
Min Jea Shin ◽  
Ki Tae Suk
Keyword(s):  
Gut Microbiota ◽  
Animal Studies ◽  
Intestinal Barrier ◽  
Intestinal Microbiome ◽  
Future Research ◽  
Pathophysiological Mechanism ◽  
Microbial Dysbiosis ◽  
Gut Barrier Function ◽  
Hepatic Diseases ◽  
Causal Nexus

Hepatocellular carcinoma (HCC), one of the leading causes of death worldwide, has a causal nexus with liver injury, inflammation, and regeneration that accumulates over decades. Observations from recent studies have accounted for the involvement of the gut–liver axis in the pathophysiological mechanism responsible for HCC. The human intestine nurtures a diversified colony of microorganisms residing in the host ecosystem. The intestinal barrier is critical for conserving the normal physiology of the gut microbiome. Therefore, a rupture of this barrier or dysbiosis can cause the intestinal microbiome to serve as the main source of portal-vein endotoxins, such as lipopolysaccharide, in the progression of hepatic diseases. Indeed, increased bacterial translocation is a key sign of HCC. Considering the limited number of clinical studies on HCC with respect to the microbiome, we focus on clinical as well as animal studies involving the gut microbiota, with the current understandings of the mechanism by which the intestinal dysbiosis promotes hepatocarcinogenesis. Future research might offer mechanistic insights into the specific phyla targeting the leaky gut, as well as microbial dysbiosis, and their metabolites, which represent key pathways that drive HCC-promoting microbiome-mediated liver inflammation and fibrosis, thereby restoring the gut barrier function.

scholarly journals Role of Gut-Microbiota in Hepatocarcinogenesis

2019 ◽  
Author(s):  
Haripriya Gupta ◽  
Gi Soo Youn ◽  
Min Jea Shin ◽  
Ki Tae Suk
Keyword(s):  
Gut Microbiota ◽  
Animal Studies ◽  
Intestinal Barrier ◽  
Intestinal Microbiome ◽  
Future Research ◽  
Pathophysiological Mechanism ◽  
Microbial Dysbiosis ◽  
Gut Barrier Function ◽  
Hepatic Diseases ◽  
Causal Nexus

Hepatocellular carcinoma (HCC), one of the leading causes of death worldwide, has a causal nexus with liver injury, inflammation, and regeneration that accumulate over decades. Observations from recent studies have accounted for the involvement of the gut-liver axis in the pathophysiological mechanism responsible for HCC. The human intestine nurtures a diversified colony of microorganisms residing in the host ecosystem. The intestinal barrier is critical for conserving the normal physiology of the gut microbiome. Therefore, a rupture of this barrier or dysbiosis cause the intestinal microbiome to serve as the main source of portal-vein endotoxins such as lipopolysaccharide, in the progression of hepatic diseases. Indeed, increased bacterial translocation is a key sign of HCC. Considering the limited number of clinical studies on HCC with respect to the microbiome, we focus on the clinical as well as animal studies involving the gut microbiota with the current understandings of the mechanism by which the intestinal dysbiosis promotes hepatocarcinogenesis. Future research might offer mechanistic insights into the specific phyla targeting the leaky gut, as well as microbial dysbiosis, and their metabolites, as key pathways that drive HCC-promoting microbiome-mediated liver inflammation and fibrosis, thereby restoring the gut barrier function.

scholarly journals Modulation of the Gut Microbiota by Shen-Yan-Fang-Shuai Formula Improves Obesity Induced by High-Fat Diets

2020 ◽  
Vol 11 ◽  
Author(s):  
Zhen Wang ◽  
Junfeng Lu ◽  
Jingwei Zhou ◽  
Weiwei Sun ◽  
Yang Qiu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Metabolic Disorders ◽  
Intestinal Barrier ◽  
Fecal Microbiota ◽  
16S Rrna Genes ◽  
Rrna Genes ◽  
Therapeutic Effects ◽  
Low Grade ◽  
High Fat ◽  
Gut Barrier Function

Obesity and related metabolic disorders are associated with intestinal microbiota dysbiosis, disrupted intestinal barrier and chronic inflammation. Shen-Yan-Fang-Shuai formula (SYFSF) is a traditional Chinese herbal formula composed of Astragali Radix, Radix Angelicae Sinensis, Rheum Officinale Baill, and four other herbs. In this study, we identified that SYFSF treatment prevented weight gain, low-grade inflammation and insulin resistance in high-fat diet (HFD)-fed mice. SYFSF also substantially improved gut barrier function, reduced metabolic endotoxemia, as well as systemic inflammation. Sequencing of 16S rRNA genes obtained from fecal samples demonstrated that SYFSF attenuated HFD-induced gut dysbiosis, seen an decreased Firmicutes to Bacteroidetes ratios. Microbial richness and diversity were also higher in the SYFSF-treated HFD group. Furthermore, similar therapeutic effects and changes in gut microbiota profile caused by SYFSF could be replicated by fecal microbiota transfer (FMT). Taken together, our study highlights the efficacy of SYFSF in preventing obesity and related metabolic disorders. Its therapeutic effect is associated with the modulation of gut microbiota, as a prebiotic.

scholarly journals Association of Hyperuricemia With Immune Disorders and Intestinal Barrier Dysfunction

2020 ◽  
Vol 11 ◽  
Author(s):  
Qiulan Lv ◽  
Daxing Xu ◽  
Xuezhi Zhang ◽  
Xiaomin Yang ◽  
Peng Zhao ◽  
...  
Keyword(s):  
Uric Acid ◽  
Gut Microbiota ◽  
Intestinal Barrier ◽  
Urate Oxidase ◽  
Intestinal Immunity ◽  
Immune Disorders ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction ◽  
Gut Barrier Function ◽  
Tnf Α

BackgroundMore than 30–40% of uric acid is excreted via the intestine, and the dysfunction of intestinal epithelium disrupts uric acid excretion. The involvement of gut microbiota in hyperuricemia has been reported in previous studies, but the changes and mechanisms of intestinal immunity in hyperuricemia are still unknown.MethodsThis study developed a urate oxidase (Uox)-knockout (Uox–/–) mouse model for hyperuricemia using CRISPR/Cas9 technology. The lipometabolism was assessed by measuring changes in biochemical indicators. Furthermore, 4-kDa fluorescein isothiocyanate–labeled dextran was used to assess gut barrier function. Also, 16S rRNA sequencing was performed to examine the changes in gut microbiota in mouse feces. RNA sequencing, Western blot, Q-PCR, ELISA, and immunohistochemical analysis were used for measuring gene transcription, the number of immune cells, and the levels of cytokines in intestinal tissues, serum, kidney, liver, pancreas, and vascellum.ResultsThis study showed that the abundance of inflammation-related microbiota increased in hyperuricemic mice. The microbial pattern recognition–associated Toll-like receptor pathway and inflammation-associated TNF and NF-kappa B signaling pathways were significantly enriched. The increased abundance of inflammation-related microbiota resulted in immune disorders and intestinal barrier dysfunction by upregulating TLR2/4/5 and promoting the release of IL-1β and TNF-α. The levels of epithelial tight junction proteins occludin and claudin-1 decreased. The expression of the pro-apoptotic gene Bax increased. The levels of LPS and TNF-α in systemic circulation increased in hyperuricemic mice. A positive correlation was observed between the increase in intestinal permeability and serum levels of uric acid.ConclusionHyperuricemia was characterized by dysregulated intestinal immunity, compromised intestinal barrier, and systemic inflammation. These findings might serve as a basis for future novel therapeutic interventions for hyperuricemia.

scholarly journals Kaempferol Alleviates Murine Experimental Colitis by Restoring Gut Microbiota and Inhibiting the LPS-TLR4-NF-κB Axis

2021 ◽  
Vol 12 ◽  
Author(s):  
Yifan Qu ◽  
Xinyi Li ◽  
Fengying Xu ◽  
Shimin Zhao ◽  
Xuemei Wu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Fecal Microbiota Transplantation ◽  
Inflammatory Diseases ◽  
Intestinal Barrier ◽  
Fluorescein Isothiocyanate ◽  
Experimental Colitis ◽  
Intestinal Microbiome ◽  
Attractive Alternative ◽  
Protective Effects ◽  
Linear Discriminant

Intestinal microbiota dysbiosis is an established characteristic of ulcerative colitis (UC). Regulating the gut microbiota is an attractive alternative UC treatment strategy, considering the potential adverse effects of synthetic drugs used to treat UC. Kaempferol (Kae) is an anti-inflammatory and antioxidant flavonoid derived from a variety of medicinal plants. In this study, we determined the efficacy and mechanism of action of Kae as an anti-UC agent in dextran sulfate sodium (DSS)-induced colitis mice. DSS challenge in a mouse model of UC led to weight loss, diarrhea accompanied by mucous and blood, histological abnormalities, and shortening of the colon, all of which were significantly alleviated by pretreatment with Kae. In addition, intestinal permeability was shown to improve using fluorescein isothiocyanate (FITC)–dextran administration. DSS-induced destruction of the intestinal barrier was also significantly prevented by Kae administration via increases in the levels of ZO-1, occludin, and claudin-1. Furthermore, Kae pretreatment decreased the levels of IL-1β, IL-6, and TNF-α and downregulated transcription of an array of inflammatory signaling molecules, while it increased IL-10 mRNA expression. Notably, Kae reshaped the intestinal microbiome by elevating the Firmicutes to Bacteroidetes ratio; increasing the linear discriminant analysis scores of beneficial bacteria, such as Prevotellaceae and Ruminococcaceae; and reducing the richness of Proteobacteria in DSS-challenged mice. There was also an evident shift in the profile of fecal metabolites in the Kae treatment group. Serum LPS levels and downstream TLR4-NF-κB signaling were downregulated by Kae supplementation. Moreover, fecal microbiota transplantation from Kae-treated mice to the DSS-induced mice confirmed the effects of Kae on modulating the gut microbiota to alleviate UC. Therefore, Kae may exert protective effects against colitis mice through regulating the gut microbiota and TLR4-related signaling pathways. This study demonstrates the anti-UC effects of Kae and its potential therapeutic mechanisms, and offers novel insights into the prevention of inflammatory diseases using natural products.

scholarly journals Roles of the Polyphenol–Gut Microbiota Interaction in Alleviating Colitis and Preventing Colitis-Associated Colorectal Cancer

2020 ◽  
Author(s):  
Yiying Zhao ◽  
Qing Jiang
Keyword(s):  
Colorectal Cancer ◽  
Animal Models ◽  
Gut Microbiota ◽  
Animal Studies ◽  
Future Research ◽  
Protective Effects ◽  
Microbial Composition ◽  
Dietary Polyphenols ◽  
Inflammatory Conditions ◽  
Opportunistic Pathogenic

ABSTRACT Accumulating evidence indicates that the gut microbiota can promote or inhibit colonic inflammation and carcinogenesis. Promotion of beneficial gut bacteria is considered a promising strategy to alleviate colonic diseases including colitis and colorectal cancer. Interestingly, dietary polyphenols, which have been shown to attenuate colitis and inhibit colorectal cancer in animal models and some human studies, appear to reach relatively high concentrations in the large intestine and to interact with the gut microbial community. This review summarizes the modulatory effects of polyphenols on the gut microbiota in humans and animals under healthy and diseased conditions including colitis and colitis-associated colorectal cancer (CAC). Existing human and animal studies indicate that polyphenols and polyphenol-rich whole foods are capable of elevating butyrate producers and probiotics that alleviate colitis and inhibit CAC, such as Lactobacillus and Bifidobacterium. Studies in colitis and CAC models indicate that polyphenols decrease opportunistic pathogenic or proinflammatory microbes and counteract disease-induced dysbiosis. Consistently, polyphenols also change microbial functions, including increasing butyrate formation. Moreover, polyphenol metabolites produced by the gut microbiota appear to have anticancer and anti-inflammatory activities, protect gut barrier integrity, and mitigate inflammatory conditions in cells and animal models. Based on these results, we conclude that polyphenol-mediated alteration of microbial composition and functions, together with polyphenol metabolites produced by the gut microbiota, likely contribute to the protective effects of polyphenols on colitis and CAC. Future research is needed to validate the causal role of the polyphenol–gut microbiota interaction in polyphenols’ anti-colitis and anti-CAC effects, and to further elucidate mechanisms underlying such interaction.

scholarly journals Comparison of the Intestinal Microbiome of Italian Patients with Multiple Sclerosis and Their Household Relatives

Life ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 620
Author(s):  
Paola Galluzzo ◽  
Fanny Claire Capri ◽  
Luca Vecchioni ◽  
Sabrina Realmuto ◽  
Luca Scalisi ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Environmental Factors ◽  
Gut Microbiota ◽  
Gut Microbiome ◽  
Intestinal Microbiome ◽  
Microbial Dysbiosis ◽  
Distinct Cluster ◽  
The Central Nervous System ◽  
Genetic And Environmental Factors ◽  
Principle Coordinate Analysis

Multiple sclerosis (MS) is a chronic immune-mediated disease of the central nervous system, caused by a combination of genetic and environmental factors. In recent years, a role in MS pathogenesis was assigned to the gut microbiota. However, different signatures of gut dysbiosis have been shown to depend on environmental factors, like diet and lifestyle. In this study, we compared the gut microbiome in MS patients and their household healthy relatives sharing lifestyle and environmental factors. Faecal metagenomic DNA was extracted and the V3–V4 regions of the conserved bacterial 16S ribosomal RNA gene were amplified and sequenced. While overall bacterial communities were similar, specific families differed between healthy and MS subjects. We observed an increase in Ruminococcaceae, Christensenellaceae, Desulfovibrionaceae, Clostridiales, and Family XIII in MS patients, while Bacteroidaceae, Tannerellaceae, Veillonellaceae, and Burkholderiaceae were more abundant in healthy controls. In addition, principle coordinate analysis showed that the gut microbiome of all MS patients formed a cluster being less diverse than the household relatives and that gut microbiota of MS patients with EDSS 4.5–7 formed a distinct cluster in respect to their controls. Overall, our study is consistent with the hypothesis that MS patients have gut microbial dysbiosis and evidenced the importance of environmental factors in shaping the gut microbiome.

scholarly journals Mycotoxin and Gut Microbiota Interactions

Toxins ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 769
Author(s):  
Philippe Guerre
Keyword(s):  
Gut Microbiota ◽  
Volatile Fatty Acids ◽  
Antimicrobial Properties ◽  
Future Research ◽  
Microbiota Composition ◽  
Toxic Compounds ◽  
Gut Barrier Function ◽  
Cell Extracts ◽  
Hydrolysis Of ◽  
Gut Microbiota Composition

The interactions between mycotoxins and gut microbiota were discovered early in animals and explained part of the differences in susceptibility to mycotoxins among species. Isolation of microbes present in the gut responsible for biotransformation of mycotoxins into less toxic metabolites and for binding mycotoxins led to the development of probiotics, enzymes, and cell extracts that are used to prevent mycotoxin toxicity in animals. More recently, bioactivation of mycotoxins into toxic compounds, notably through the hydrolysis of masked mycotoxins, revealed that the health benefits of the effect of the gut microbiota on mycotoxins can vary strongly depending on the mycotoxin and the microbe concerned. Interactions between mycotoxins and gut microbiota can also be observed through the effect of mycotoxins on the gut microbiota. Changes of gut microbiota secondary to mycotoxin exposure may be the consequence of the antimicrobial properties of mycotoxins or the toxic effect of mycotoxins on epithelial and immune cells in the gut, and liberation of antimicrobial peptides by these cells. Whatever the mechanism involved, exposure to mycotoxins leads to changes in the gut microbiota composition at the phylum, genus, and species level. These changes can lead to disruption of the gut barrier function and bacterial translocation. Changes in the gut microbiota composition can also modulate the toxicity of toxic compounds, such as bacterial toxins and of mycotoxins themselves. A last consequence for health of the change in the gut microbiota secondary to exposure to mycotoxins is suspected through variations observed in the amount and composition of the volatile fatty acids and sphingolipids that are normally present in the digesta, and that can contribute to the occurrence of chronic diseases in human. The purpose of this work is to review what is known about mycotoxin and gut microbiota interactions, the mechanisms involved in these interactions, and their practical application, and to identify knowledge gaps and future research needs.

The Gut–Liver Axis in the Control of Energy Metabolism and Food Intake in Animals

2020 ◽  
Vol 8 (1) ◽  
pp. 295-319 ◽  
Author(s):  
Robert Ringseis ◽  
Denise K. Gessner ◽  
Klaus Eder
Keyword(s):  
Energy Metabolism ◽  
Food Intake ◽  
Gut Microbiota ◽  
Metabolic Pathways ◽  
Intestinal Barrier ◽  
Short Chain Fatty Acids ◽  
Peripheral Tissues ◽  
Communication Signals ◽  
Microbial Dysbiosis ◽  
Hypothalamic Inflammation

Recent research has convincingly demonstrated a bidirectional communication axis between the gut and liver that enables the gut microbiota to strongly affect animals’ feeding behavior and energy metabolism. As such, the gut–liver axis enables the host to control and shape the gut microbiota and to protect the intestinal barrier. Gut microbiota–host communication is based on several gut-derived compounds, such as short-chain fatty acids, bile acids, methylamines, amino acid–derived metabolites, and microbial-associated molecular patterns, which act as communication signals, and multiple host receptors, which sense the signals, thereby stimulating signaling and metabolic pathways in all key tissues of energy metabolism and food intake regulation. Disturbance in the microbial ecosystem balance, or microbial dysbiosis, causes profound derangements in the regulation of appetite and satiety in the hypothalamic centers of the brain and in key metabolic pathways in peripheral tissues owing to intestinal barrier disruption and subsequent induction of hepatic and hypothalamic inflammation.

scholarly journals Translocation of gut microbiota in liver cirrhosis: mechanisms, clinical significance, and markers

2021 ◽  
Vol 23 (2) ◽  
pp. 147-160
Author(s):  
Dmitrii I. Gavrilenko ◽  
N.N. Silivontchik
Keyword(s):  
Liver Cirrhosis ◽  
Gut Microbiota ◽  
Adaptive Immunity ◽  
Clinical Significance ◽  
Bacterial Translocation ◽  
Intestinal Microbiome ◽  
Future Research ◽  
C Reactive Protein ◽  
Innate And Adaptive Immunity ◽  
Reactive Protein

This article is an overview of the data on bacterial intestinal translocation. The article reviews changes in the intestinal microbiome, the local physiological barrier, as well as the innate and adaptive immunity characteristics contributing to the liver cirrhosis development and progression. The results of published studies on the assessment of potential bacterial translocation markers (C-reactive protein, procalcitonin, lipopolysaccharide, presepsin etc.) and their use to predict infection and mortality in patients with liver cirrhosis are presented. The up-to-date methods to study the intestinal microbiome as well as some directions for future research are also described.

scholarly journals Effects of Polyphenols in Tea (Camellia sinensis sp.) on the Modulation of Gut Microbiota in Human Trials and Animal Studies

2021 ◽  
Vol 12 (2) ◽  
pp. 202-216
Author(s):  
Mus Azza Suhana Khairudin ◽  
Abbe Maleyki Mhd Jalil ◽  
Napisah Hussin
Keyword(s):  
Gut Microbiota ◽  
Beta Diversity ◽  
Animal Studies ◽  
Tea Polyphenols ◽  
Microbiota Composition ◽  
Polyphenol Compounds ◽  
Human Trials ◽  
Diet Induced Obesity ◽  
Different Types ◽  
Meta Analyses

A diet high in polyphenols is associated with a diversified gut microbiome. Tea is the second most consumed beverage in the world, after water. The health benefits of tea might be attributed to the presence of polyphenol compounds such as flavonoids (e.g., catechins and epicatechins), theaflavins, and tannins. Although many studies have been conducted on tea, little is known of its effects on the trillions of gut microbiota. Hence, this review aimed to systematically study the effect of tea polyphenols on the stimulation or suppression of gut microbiota in humans and animals. It was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) protocol. Articles were retrieved from PubMed and Scopus databases, and data were extracted from 6 human trials and 15 animal studies. Overall, large variations were observed in terms of microbiota composition between humans and animals. A more consistent pattern of diversified microbiota was observed in animal studies. Tea alleviated the gut microbiota imbalance caused by high-fat diet-induced obesity, diabetes, and ultraviolet-induced damage. The overall changes in microbiota composition measured by beta diversity analysis showed that tea had shifted the microbiota from the pattern seen in animals that received tea-free intervention. In humans, a prebiotic-like effect was observed toward the gut microbiota, but these results appeared in lower-quality studies. The beta diversity in human microbiota remains intact despite tea intervention; supplementation with different teas affects different types of bacterial taxa in the gut. These studies suggest that tea polyphenols may have a prebiotic effect in disease-induced animals and in a limited number of human interventions. Further intervention is needed to identify the mechanisms of action underlying the effects of tea on gut microbiota.

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